The role of B-1 cells in inflammation

被引:82
作者
Aziz, Monowar [1 ]
Holodick, Nichol E. [2 ]
Rothstein, Thomas L. [2 ]
Wang, Ping [1 ,3 ]
机构
[1] Feinstein Inst Med Res, Ctr Translat Res, Manhasset, NY 11030 USA
[2] Feinstein Inst Med Res, Ctr Oncol & Cell Biol, Manhasset, NY 11030 USA
[3] Hofstra North Shore LIJ Sch Med, Dept Surg, Manhasset, NY 11030 USA
基金
美国国家卫生研究院;
关键词
B-1; cells; Natural IgM; Inflammation; Autoimmunity; Influenza; Sepsis; Atherosclerosis; IBD; REGULATORY B-CELLS; B10; CELLS; INFLUENZA-VIRUS; NATURAL IGM; IMMUNOGLOBULIN-M; MARGINAL ZONE; SEVERE SEPSIS; DILATED CARDIOMYOPATHY; ULCERATIVE-COLITIS; INNATE;
D O I
10.1007/s12026-015-8708-3
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
B-1 lymphocytes exhibit unique phenotypic, ontogenic, and functional characteristics that differ from the conventional B-2 cells. B-1 cells spontaneously secrete germline-like, repertoire-skewed polyreactive natural antibody, which acts as a first line of defense by neutralizing a wide range of pathogens before launching of the adaptive immune response. Immunomodulatory molecules such as interleukin-10, adenosine, granulocyte-macrophage colony-stimulating factor, interleukin-3, and interleukin-35 are also produced by B-1 cells in the presence or absence of stimulation, which regulate acute and chronic inflammatory diseases. Considerable progress has been made during the past three decades since the discovery of B-1 cells, which has improved not only our understanding of their phenotypic and ontogenic uniqueness but also their role in various inflammatory diseases including influenza, pneumonia, sepsis, atherosclerosis, inflammatory bowel disease, autoimmunity, obesity and diabetes mellitus. Recent identification of human B-1 cells widens the scope of this field, leading to novel innovations that can be implemented from bench to bedside. Among the vast number of studies on B-1 cells, we have carried out a literature review highlighting current trends in the study of B-1 cell involvement during inflammation, which may result in a paradigm shift toward sustainable therapeutics in various inflammatory diseases.
引用
收藏
页码:153 / 166
页数:14
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